(Circulation. 1997;96:4261-4267.)
© 1997 American Heart Association, Inc.
Articles |
Direct Intracoronary Evidence of Collateral Steal in Humans
From Cardiology, University Hospital, Bern, Switzerland.
Correspondence to PD Dr Christian Seiler, MD, FESC, University Hospital, Cardiology, Inselspital, Freiburgstr, Bern, Switzerland. E-mail christian.seiler{at}insel.ch
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Abstract |
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Background Coronary steal is defined as a fall in blood flow toward a certain vascular region in favor of another area during arteriolar vasodilatation, ie, a coronary flow velocity reserve (CFVR) <1. The purpose of this study was to determine the frequency of steal in patients with a wide range of collateral supply to a vascular area of interest and to assess whether steal is associated with the amount of collateral flow.
Methods and Results One hundred patients 57±9 years old with a coronary artery stenosis to be dilated were examined with intracoronary (IC) Doppler guidewires. IC adenosine–induced CFVR<1 obtained distal to the stenosis was defined as steal. An index for collateral flow was determined by positioning the Doppler guidewire in the collateral-dependent vessel distal to the stenosis and measuring the flow velocity time integral during (Vioccl, cm) and after (Viø-occl) balloon occlusion. Vioccl/Viø-occl was determined without and with intravenous adenosine (140 µg · kg-1 · min-1). Coronary steal occurred in 10 of 100 patients. Patients with steal showed superior collaterals compared with those without steal: Vioccl/Viø-occl=0.65±0.24 in patients with steal versus 0.29±0.18 in those without steal (P=.0001). In all patients with steal, there was a reduction in collateral flow during intravenous adenosine–induced hyperemia, whereas in the majority (70%) of patients without steal, collateral flow increased or remained unchanged during hyperemia.
Conclusions Coronary steal assessed by intracoronary Doppler flow velocity measurements occurs in 10% of patients with a wide range of coronary collaterals to the vascular area from which blood flow is redistributed. There is a direct association between the presence of steal away from and the amount of collateral flow toward the region under investigation. Collateral flow to the vascular region studied decreases during adenosine-induced hyperemia, which indicates a mechanism of steal via the extensive collaterals.
Key Words: coronary disease • collateral circulation • regional blood flow • steal • adenosine
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The coronary collateral circulation is an alternative source of blood supply to the myocardium jeopardized by the failure of the original stenotic or occluded vessel to provide adequate blood flow to this region. The functional relevance of coronary collaterals in humans has been debated for many years.1–3 Numerous studies have demonstrated a protective role of collaterals in hearts with CAD, showing smaller infarcts,4 less ventricular aneurysm formation, improved ventricular function,4,5 and better survival3 compared with patients in whom collaterals were not visualized. Conversely, it has been stated that "coronary collaterals in man are more an indication of severe regional ischemia than a sign of biological 'compensation' for a perfusion deficit."6 Furthermore, some reports have suggested negative aspects of well-developed versus poorly developed coronary collaterals, such as more frequent restenosis after angioplasty of atherosclerotic lesions proximal to a vascular region with good collateralization.7 The beneficial effect of nifedipine on variables of myocardial ischemia has been demonstrated to be impaired in patients with "good" collaterals,8 and it has been suggested that a redistribution of blood via collaterals away from the myocardial area in need could be one of the mechanisms responsible for the proischemic complications related to dihydropyridine calcium channel blockers.9 These variations in regional blood flow under conditions of microvascular dilatation are called coronary artery steal, and they are estimated to occur in 10% to 30% of patients with CAD undergoing dipyridamole stress testing and nuclear perfusion imaging.10 Steal is defined as an absolute or relative fall in coronary blood flow to a certain vascular region in favor of another supply area under conditions of hyperemia, ie, a coronary flow reserve of <110,11 (Fig 1
). The
mechanism for this redistribution of blood flow can be a fall in
perfusion pressure at the origin of collateral vessels due to proximal
stenoses of coronary arteries supplying the collaterals
or due to proximal viscous friction developing at high-flow states even
in normal coronary arteries from which the collaterals
arise.12–14 There are different categories of
coronary steal, ie, steal via collaterals, "vertical" steal
between different layers of the myocardium,10
and coronary artery branch steal among adjacent vascular areas
originating from a common branch bifurcation.11
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So far, direct documentation of steal has been possible only experimentally.12–14 With the advent of small intravascular Doppler angioplasty guidewires (0.014 in, 0.33 mm in diameter), it has become feasible to directly verify the consistent but indirect and qualitative findings of noninvasive methods on pharmacologically induced steal phenomena.15,16 Thus, the purpose of this study was (1) to document coronary steal, (2) to determine its frequency in a patient population with CAD and a wide spectrum of collateral supply, and (3) to assess the relation between steal and the amount of collateral supply to the vascular region under investigation.
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Methods |
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Patients
One hundred patients (57±9 years old; 21 men, 79 women) with one- or two-vessel CAD were included in this study. All of them underwent PTCA because of CAD-related symptoms of at least one stenotic lesion.
The present investigation was approved by the institutional ethics committee, and the patients gave informed consent to participate in the study.
The study population was divided into two groups according to the
presence of coronary steal distal to the coronary
stenosis undergoing PTCA ("steal" group, ie, CFVR
determined by intracoronary Doppler flow wires <1 obtained
three times repetitively; Fig 2) and
according to absent coronary steal ("no steal" group, ie,
CFVR
1).
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Cardiac Catheterization and Coronary
Angiography
Patients underwent left heart catheterization
for diagnostic purposes. Premedication consisted of 10 mg
chlordiazepoxide administered orally 1 hour before the procedure.
Aortic pressure was measured with the PTCA guiding catheter. Biplane
left ventricular angiography was performed in all patients,
followed by diagnostic coronary angiography.
Coronary artery stenosis severities were estimated
qualitatively as percent diameter stenosis. Angiographic
collateral degrees (0 to 3) were determined according to the extent of
epicardial coronary artery filling via collaterals with
contrast medium from the contralateral side: 0, no filling of the
ipsilateral vessel via collaterals from the contralateral side; 1,
small side branches filled; 2, major side branches of the main
epicardial vessel filled; and 3, main epicardial vessel filled by
collaterals from the contralateral side.17
Intracoronary Doppler Flow Velocity
Measurements
IC Doppler flow velocity measurements were performed with a
0.014-in (0.33-mm diameter) PTCA Doppler guidewire with a 12-MHz
piezoelectric crystal at its tip (FloWire, formerly Cardiometrics Inc,
now Endosonics). This Doppler guidewire has recently been validated
and, compared with electromagnetic flowmeters, has been shown to
measure phasic flow velocity patterns accurately and to track changes
in flow rate linearly.18
CFVR values were determined by dividing maximum hyperemic peak
flow velocity averaged over three consecutive cardiac cycles (APV) by
APV during resting conditions. Hyperemia was induced
pharmacologically with either IC bolus injection of 18 µg
adenosine for the left coronary artery and 12 µg
adenosine for the right coronary artery or
intravenous infusion at a rate of 140 µg ·
min-1 · kg-1 body mass.19
An index of coronary collateral flow to the balloon-occluded
vascular region of interest relative to normal resting flow during
vessel patency, ie, after completed
revascularization, was determined as the ratio of
flow velocity time integral distal to the occluded stenosis
(Vioccl, cm) divided by that obtained at the identical
location after PTCA (ie, not occluded, Viø-occl, cm):
Vioccl/Viø-occl (Fig 3).20 In patients who showed
bidirectional flow velocity signals (Fig 3), the ratio between
antegrade and retrograde flow velocities was identified as the absolute
flow velocity.
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Study Protocol
After diagnostic coronary angiography, an
interval of at least 10 minutes was allowed for dissipation of the
effect of the nonionic contrast medium (iopamidol 755 mg/mL) on
coronary flow velocity and vasomotion. An IC bolus of 0.2 mg
nitroglycerin was given to maintain epicardial
coronary artery calibers constant and thus to prevent the
influence of changing epicardial vessel diameters on CFVR
measurements.21 CFVR measurements were obtained proximal
and at least three times distal to the stenosis to be dilated.
Repetitive distal CFVR measurements were averaged. After distal CFVR
measurements, the distal flow velocity time integral,
Vioccl, was determined repetitively during balloon
occlusion without intravenous adenosine. During
balloon inflation, the occurrence of chest pain and ischemic
changes on the IC ECG22 were observed. After balloon
deflation and cessation of reactive hyperemia, occlusive distal
Vioccl was determined during adenosine infusion
after a 10 mm Hg systolic blood pressure decrease. Blood
pressure and heart rate were recorded continuously during all flow
velocity measurements, including nonocclusive, "normal" flow
velocity time integral Viø-occl at the same distal
location as Vioccl, the former of which was recorded
after completion of PTCA and after cessation of reactive
hyperemia.
Statistical Analysis
Between-group comparison of demographic, angiographic,
hemodynamic, and Doppler flow velocity data were
performed by an unpaired two-sided Student's t test.
Hemodynamic data during different time points among
patients of the same group were analyzed with a paired
t test. A 
2 test was used for comparison of
categorical variables between the two study groups. Linear
regression analysis was applied for analysis of an
association between collateral flow indices and intravenous
adenosine–induced change in the indices. Statistical
significance was defined at a value of P<.05.
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Results |
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Patient Characteristics
The entire study population comprised 100 patients 57±9 years old: 10 were in the group with coronary steal, and 90 showed no steal. There were no statistically significant differences among the two groups regarding the patients' age, sex, hemodynamic variables during diagnostic cardiac catheterization such as heart rate and blood pressure, number of coronary arteries with stenotic lesions on the coronary angiogram, left ventricular angiographic ejection fraction, and the coronary artery with the stenotic lesion to be dilated (ie, the index stenosis; Table 1
).
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Angiographic Data
Patients revealing a coronary steal phenomenon had a more
severe index stenosis than those without steal: 91±10% versus
79±16% diameter stenosis (P=.04; Table 1
). Among
patients with a two-vessel CAD, the diameter stenosis of the
lesion of the contralateral, collateral-supplying vessel was 50±55%
in the group with steal and 31±65% in the group without steal
(P=NS). Complete occlusion of the stenoses under
consideration occurred more often in patients with steal than in those
without (Table 1). Proximal location of the stenosis to be
dilated was found in 7 of 10 patients with steal and in 40 of 90
patients without steal (P<.05). During balloon occlusion of
the stenosis to be dilated, patients with coronary
steal suffered from angina pectoris significantly less often and showed
signs of myocardial ischemia on IC ECG less often than those
without steal (Table 2). Angiographic
collateral degree was 2.4±0.6 in the group with steal and 1.0±0.8 in
the group without steal (P=.0001).
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Doppler Flow Velocity Data
In agreement with the definition of coronary steal
(CFVR<1), CFVR measured via the Doppler flow velocity guidewire
distal to the index stenosis before PTCA was 0.7±0.5 among
patients with steal and 1.9±0.7 among those without steal
(P=.0001; Table 2). Doppler-derived IC collateral flow
index (Vioccl/Viø-occl) at rest (ie, without
intravenous adenosine–induced hyperemia or
microvascular dilatation) obtained distal to the stenosis and
calculated as the flow velocity time integral (Vi, cm) during balloon
occlusion of the stenosis (Vioccl, cm) divided by
Vi after completed PTCA and after cessation of postocclusive
hyperemia (Viø-occl, cm) was significantly higher
in patients with steal than in those without steal (Fig 4). The
Vioccl/Viø-occl values at rest measured in the
groups with and without steal indicate that collaterals from the
contralateral side to the vascular region of interest provide 65% and
29%, respectively, of the normal blood flow via the revascularized
ipsilateral coronary artery.
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) and without (
) coronary steal without and with
intravenous adenosine–induced hyperemia.
Vioccl/Viø-occl=0.6 means that during
occlusion, collaterals provide 60% of flow through revascularized,
open vessel. During baseline conditions (ie, without
intravenous adenosine), patients with steal show a
greater Vioccl/Viø-occl than those without
steal. This difference is no longer present during
hyperemia with intravenous adenosine.
During hyperemia, Vioccl/Viø-occl
decreases significantly in patients with steal, whereas it remains
unchanged in those without steal. IV indicates
intravenous.
Association Between Collateral Flow Index and Steal
Determination of collateral flow index during
intravenous adenosine–induced hyperemia
compared with resting conditions showed reduced values of
Vioccl/Viø-occl in all the patients with steal
but increased or constant Vioccl/Viø-occl in
70% of the patients without steal (Fig 4). The standard for steal
defined as CFVR<1 could be predicted by a fall in
Vioccl/Viø-occl during hyperemia with
100% sensitivity and 70% specificity. Presence of steal, ie, CFVR<1,
was significantly associated with a fall in the flow index via the
collaterals, and absence of steal was, on average, associated with an
unchanged collateral flow index (Fig 4 and Table 3). Hemodynamic
variables such as mean aortic pressure and heart rate changed
similarly in response to adenosine infusion between the two
study groups (Table 3). In both groups, there was an 
10 mm Hg
decrease of mean aortic pressure (P<.03) but no significant
increase in heart rate.
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Fig 5 illustrates that there is an
inverse relation between the collateral flow index at resting
conditions (ie, without intravenous adenosine) and
its capacity to increase during intravenous
adenosine–induced hyperemia.
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, those without
steal. |
Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This study in 100 patients with CAD provides direct intracoronary evidence of blood flow redistribution during hyperemia away from a collateralized vascular region toward a contralateral, collateral-supplying area, ie, it documents coronary steal in humans for the first time by intravascular Doppler measurements. Among those patients with a wide range of collateral supply to the vascular region studied, coronary steal occurred in 10%. A strong direct association between the presence and the degree of steal away from and the amount of collaterals toward the collateralized vascular territory was found.
Evidence and Occurrence of Steal
The phenomenon of coronary steal has been recognized for
more than 25 years,12,23 and it has been studied
experimentally,13–15,24,25 suspected
clinically,8,26 modeled theoretically,27 and
recently demonstrated by PET in humans.15 So far, direct
intracoronary evidence has been provided only in two case
reports.28,29
Data from the literature on the proischemic effect of the
calcium antagonist nifedipine due to suspected
coronary steal may serve to estimate the occurrence of this
phenomenon found in 10% of the present study population: an
increased nifedipine-induced exertional ST-segment
depression or exacerbation of anginal symptoms was detected by Loos and
Kaltenbach30 in 6% of the patients, by Kober et
al31 in 20%, by Stone et al32 in 14%, and by
Schulz and coworkers26 in 10% to 20%. Of 1100 cardiac PET
studies in patients with collateralized, occluded vascular territories,
75 (ie, 7%) revealed coronary steal.10
The rather small difference in the frequency of coronary steal among this and other investigations is probably accidental but may, on the other hand, be explained by the widely varying, predominantly indirect methods to detect steal. Furthermore, it may reflect some of the controversy that existed and may be revived by the present data on the coronary morphological conditions necessary to cause steal.
Coronary Steal and the Collateral Circulation
Coronary steal can be defined as a fall in absolute
coronary perfusion of collateralized myocardium
after coronary arteriolar vasodilation, ie, myocardial
perfusion reserve <1. The definition of steal we chose is slightly
different: an index for vascular flow rate reserve, CFVR, of <1
established coronary steal. As long as the epicardial
coronary artery caliber is maintained constant by
nitroglycerin before the capacity to increase flow is
measured, CFVR can be used instead of the CFR for the functional
assessment of the coronary circulation without introducing a
substantial error.21 However, Gould has asserted that CFR
does not correspond to myocardial perfusion reserve at values <1,
because "... arterial CFR of less than one does not
occur... ."33 This investigation was designed in its
present form at the moment when a CFVR<1 could be documented by an
intracoronary Doppler guidewire positioned distal to a
stenotic lesion after balloon dilatation and stent
implantation, thus excluding the possibility of a collapsing
stenosis as the cause of a CFVR<1.34 Nevertheless,
the possibility cannot be disregarded that elasticity of some of the
stenoses under investigation may have partly influenced the
results of this study.
The coronary structural conditions for the occurrence of steal
were controversial34,35 before Becker13
demonstrated in dogs that dipyridamole-induced
coronary steal occurs if collateral vessels supply
myocardium downstream of coronary occlusions and
even more so, if the collateral-providing vessel is proximally
stenotic. Patterson and Kirk14 corroborated those
data by showing in dogs with an occluded LAD collateralized via the LCx
that increments of vascular resistance proximal to the origin of the
collaterals caused a linear increase in the magnitude of
coronary steal. However, a certain degree of steal could be
observed even in the absence of a stenotic lesion upstream of
the collateral-supplying artery. In their analysis of a general
network model simulating the collateralized coronary
circulation (ie, a Wheatstone bridge model), Demer and
coworkers27 predicted the occurrence of coronary
steal, ie, myocardial perfusion reserve <1, provided that collaterals
from the LCx (with a 60% proximal cross-sectional area
stenosis) to an occluded LAD conducted >1% of blood relative
to normal maximal coronary conductance. Furthermore, assuming a
collateral capacity sufficient to provide normal resting
coronary flow in the occluded LAD, ie, 20% collateral
conductance, that study estimated that steal begins to take place in
the presence of a 20% vascular lumen area reduction of the LCx
supplying the collaterals.
Thus, it appears unambiguous that the following qualitative elements
are indispensable for the occurrence of collateral steal: an occluded
or at least highly obstructed coronary artery, coronary
collaterals supplying this vessel with blood from a contralateral
artery, and a collateral-supplying artery that itself is more or less
obstructed proximal to the collaterals (see also Fig 1). The results of
the present intravascular Doppler study indicate the presence
of all those elements in patients who show coronary steal.
There is an association between the qualitative degree of collateral
supply to the region of interest and the occurrence of steal from it,
ie, patients with coronary steal suffered from angina pectoris
less often and showed signs of myocardial ischemia on an
intracoronary ECG during stenosis occlusion less often
than individuals without steal. An intracoronary Doppler
flow velocity–derived index of collateral flow also revealed a
quantitative relation between the occurrence of steal and the resting
flow through collaterals relative to the antegrade flow after the
revascularization of the vessel studied (Fig 4).
The Doppler-derived collateral flow index has been demonstrated to
accurately distinguish between collaterals to a balloon-occluded
vascular region supplying sufficient or insufficient blood flow to this
area to prevent myocardial ischemia.20 A reduction
of 40% in (occlusive) collateral flow during
intravenous adenosine in all the patients with
steal (Fig 4) further indicates a mechanism of steal via the extensive
collaterals and not through local redistribution via a coronary
branch adjacent to that under investigation taking off from a common
bifurcation (ie, coronary artery branch steal11).
The inverse association between collateral flow and the decrease of
flow during adenosine-induced arteriolar dilatation (Fig 5)
corroborates the notion27 of increasing steal with
augmented collateral conductance. However, some aspects of
coronary structural characteristics among patients with steal
vary from the cited literature, namely, the presence of steal in cases
without complete occlusion of the coronary artery under
investigation and the finding that steal may occur in patients without
stenotic lesions of the collateral-supplying artery. In
addition, the collateral flow necessary to serve as a condition for the
occurrence of steal is probably much larger than that indicated above
(1%),27 and it is possibly as high as 30% to 40% of
normal resting flow. Thus, it may be that only patients with a
collateral supply to a vascular region sufficient to prevent myocardial
infarction at rest20 are at risk to develop
coronary steal via these collaterals during
hyperemia.
Study Limitations
In principle, it is possible that flow velocity signals may not be
recorded during coronary occlusion because of obstruction
of collaterals through the inflated PTCA balloon or because of
malpositioning of the Doppler guidewire with its tip directed
against the vessel wall. In the present study, this may have
occurred by chance more often during intravenous
adenosine than during the first stenosis occlusion,
thereby at least partly accounting for the wide variety of collateral
flow velocity responses in the no-steal group. However, it would not
have changed the incidence of steal, because steal was defined on the
basis of CFVR and not of changes in collateral flow in response to
adenosine. Conversely, the question can be raised in this
context as to whether steal may be occurring in patients showing a
nonartificial fall in collateral flow during hyperemia in the
presence of a CFVR >1, a theoretical possibility that cannot be
further elucidated based on the design of this study.
Clinical Implications of Steal
The presence of coronary steal most often indicates
extensive collateral supply to the vascular region under examination
and therefore most likely viable myocardium.
Coronary steal in the absence of large collaterals is probably
quite infrequent,10 and it may be due to
hyperemia-induced phenomena of "vertical" blood flow
redistribution between epicardial and endocardial
vessels10 or to diversion of blood at a coronary
artery bifurcation showing certain atherosclerotic morphological
changes.11 By attesting to a well-developed collateral
circulation, coronary steal may also suggest that after balloon
dilatation of a stenosis, there could be flow via collaterals
to the region distal to it competing for the antegrade flow and thus
heightening the risk for restenosis.7 It can be
speculated that collateral steal may be one of the reasons for an
inadequate functional result after PTCA, because the impact of
hyperemia-induced flow diversion may continue even after
completed revascularization.29 In the
context of collateral steal, the necessity or adequacy of PTCA,
particularly in patients with complete occlusions, may even be
questioned, and alternative treatment strategies can be considered,
such as medical therapy with ß-blocking agents, which have been
demonstrated to reduce the incidence of myocardial ischemic
episodes independent of coronary collateral
flow.8
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported by a grant from the Swiss Heart Foundation and by a grant from the Swiss National Science Foundation, grant 32–49623.96.
Received June 5, 1997; revision received August 22, 1997; accepted September 7, 1997.
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  R Vogel, A Indermuhle, P Meier, and C Seiler Quantitative stress echocardiography in coronary artery disease using contrast-based myocardial blood flow measurements: prospective comparison with coronary angiography Heart, March 1, 2009; 95(5): 377 - 384. [Abstract] [Full Text] [PDF]
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 G. Heusch and R. Schulz The role of heart rate and the benefits of heart rate reduction in acute myocardial ischaemia Eur. Heart J. Suppl., September 1, 2007; 9(suppl_F): F8 - F14. [Abstract] [Full Text] [PDF]
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 G. S. Werner, M. Fritzenwanger, D. Prochnau, G. Schwarz, M. Ferrari, W. Aarnoudse, N. H.J. Pijls, and H. R. Figulla Determinants of Coronary Steal in Chronic Total Coronary Occlusions: Donor Artery, Collateral, and Microvascular Resistance J. Am. Coll. Cardiol., July 4, 2006; 48(1): 51 - 58. [Abstract] [Full Text] [PDF]
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M. J. Kern Walking With Sir William: Reflections on Collateral Steal, Recruitment, and Ischemic Protection J. Am. Coll. Cardiol., July 4, 2006; 48(1): 66 - 69. [Full Text] [PDF]
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 P. Voci, F. Pizzuto, and F. Romeo Coronary flow: a new asset for the echo lab? Eur. Heart J., November 1, 2004; 25(21): 1867 - 1879. [Full Text] [PDF]
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C. Seiler The human coronary collateral circulation Heart, November 1, 2003; 89(11): 1352 - 1357. [Full Text] [PDF]
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 G. S. Werner and H. R. Figulla Direct Assessment of Coronary Steal and Associated Changes of Collateral Hemodynamics in Chronic Total Coronary Occlusions Circulation, July 23, 2002; 106(4): 435 - 440. [Abstract] [Full Text] [PDF]
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J.-P. Bin, E. Le, R. A. Pelberg, M. P. Coggins, K. Wei, and S. Kaul Mechanism of Inducible Regional Dysfunction During Dipyridamole Stress Circulation, July 2, 2002; 106(1): 112 - 117. [Abstract] [Full Text] [PDF]
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S. A. J. Chamuleau, R. A. Tio, C. C. de Cock, E. D. de Muinck, N. H. J. Pijls, B. L. F. van Eck-Smit, K. T. Koch, M. Meuwissen, M. G. W. Dijkgraaf, A. de Jong, et al. Prognostic value of coronary blood flow velocity and myocardial perfusion in intermediate coronary narrowings and multivessel disease J. Am. Coll. Cardiol., March 6, 2002; 39(5): 852 - 858. [Abstract] [Full Text] [PDF]
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T. Pohl, C. Seiler, M. Billinger, E. Herren, K. Wustmann, H. Mehta, S. Windecker, F. R. Eberli, and B. Meier Frequency distribution of collateral flow and factors influencing collateral channel development: Functional collateral channel measurement in 450 patients with coronary artery disease J. Am. Coll. Cardiol., December 1, 2001; 38(7): 1872 - 1878. [Abstract] [Full Text] [PDF]
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T Pohl, P Hochstrasser, M Billinger, M Fleisch, B Meier, and C Seiler Influence on collateral flow of recanalising chronic total coronary occlusions: a case-control study Heart, October 1, 2001; 86(4): 438 - 443. [Abstract] [Full Text] [PDF]
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 M. Billinger, M. Fleisch, F. R. Eberli, B. Meier, and C. Seiler Collateral and collateral-adjacent hyperemic vascular resistance changes and the ipsilateral coronary flow reserve: Documentation of a mechanism causing coronary steal in patients with coronary artery disease Cardiovasc Res, February 16, 2001; 49(3): 600 - 608. [Abstract] [Full Text] [PDF]
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O. O. Akinboboye, O. Idris, R.-L. Chou, R. R. Sciacca, P. J. Cannon, and S. R. Bergmann Absolute quantitation of coronary steal induced by intravenous dipyridamole J. Am. Coll. Cardiol., January 1, 2001; 37(1): 109 - 116. [Abstract] [Full Text] [PDF]
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 D. Belhomme, J. Peynet, E. Florens, O. Tibourtine, M. Kitakaze, and P. Menasche Is adenosine preconditioning truly cardioprotective in coronary artery bypass surgery? Ann. Thorac. Surg., August 1, 2000; 70(2): 590 - 594. [Abstract] [Full Text] [PDF]
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S. Tommasi, E. Carluccio, M. Bentivoglio, L. Corea, and E. Picano Low-dose dipyridamole infusion acutely increases exercise capacity in angina pectoris: A double-blind, placebo controlled crossover stress echocardiographic study J. Am. Coll. Cardiol., January 1, 2000; 35(1): 83 - 88. [Abstract] [Full Text] [PDF]
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C. Seiler, M. Fleisch, M. Billinger, and B. Meier Simultaneous intracoronary velocity- and pressure-derived assessment of adenosine-induced collateral hemodynamics in patients with one- to two-vessel coronary artery disease J. Am. Coll. Cardiol., December 1, 1999; 34(7): 1985 - 1994. [Abstract] [Full Text] [PDF]
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M. Billinger, M. Fleisch, F. R. Eberli, A. Garachemani, B. Meier, and C. Seiler Is the development of myocardial tolerance to repeated ischemia in humans due to preconditioning or to collateral recruitment? J. Am. Coll. Cardiol., March 15, 1999; 33(4): 1027 - 1035. [Abstract] [Full Text] [PDF]
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T. Tanaka, M. Fujita, I. Nakae, S.-I. Tamaki, K. Hasegawa, Y. Kihara, R. Nohara, and S. Sasayama Improvement of exercise capacity by sarpogrelate as a result of augmented collateral circulation in patients with effort angina J. Am. Coll. Cardiol., December 1, 1998; 32(7): 1982 - 1986. [Abstract] [Full Text] [PDF]
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C. Seiler, M. Billinger, R. Bolli, M. M. Leesar, M. M. Ahmed, M. M. Stoddard, and M. J. Broadbent Adenosine-Induced Preconditioning of Human Myocardium? • Response Circulation, August 25, 1998; 98(8): 824 - 825. [Full Text]
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 S. Windecker, Y. Allemann, M. Billinger, T. Pohl, D. Hutter, T. Orsucci, L. Blaga, B. Meier, and C. Seiler Effect of endurance training on coronary artery size and function in healthy men: an invasive followup study Am J Physiol Heart Circ Physiol, June 1, 2002; 282(6): H2216 - H2223. [Abstract] [Full Text] [PDF]
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